Mechanistic insights into the pathogenesis and management of acute pancreatitis

Haidy E. Michel, Naglaa Gamal, M. Tadros
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Abstract

Acute pancreatitis (AP) is an inflammatory disorder of the pancreas; its incidence rate is increasing worldwide; it is around 34 cases per 100,000 persons /year. It may range from mild to severe cases and may be associated with morbidity and mortality mainly due to multiple organ dysfunction syndromes (MODS). Till now, there is no specific therapy for the disease and the treatment of AP is mainly supportive. Moreover, the underlying mechanisms included in its pathogenesis are not fully clear. However, it may include oxidative stress and inflammatory response, including critical mediators, such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), toll-like receptor-4 (TLR-4), nuclear factor-kappa B (NF-κB), and high-mobility group box protein1 (HMGB1). Thus, there is a pressing need for continuous search in this era to clarify different pathogenesis and the development of new treatment options for AP, also understanding the disease. While research on the human pancreas remains challenging, animal models of AP may help to elucidate the disease pathophysiology & to discover new target options for the development of new therapies. This review aims to revise several aspects related to AP diagnosis and management and to summarize different animal models of AP.
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急性胰腺炎的发病机制和治疗
急性胰腺炎(AP)是胰腺的炎症性疾病;其发病率在世界范围内呈上升趋势;每年每10万人中约有34例。它可能从轻度到重度不等,并可能与发病率和死亡率相关,主要是由于多器官功能障碍综合征(MODS)。到目前为止,该疾病还没有特异性的治疗方法,AP治疗主要是支持性的。此外,其发病机制尚不完全清楚。然而,它可能包括氧化应激和炎症反应,包括关键介质,如白细胞介素-1β (IL-1β)、肿瘤坏死因子-α (TNF-α)、toll样受体-4 (TLR-4)、核因子-κB (NF-κB)和高迁移率组盒蛋白1 (HMGB1)。因此,迫切需要在这个时代进行持续的研究,以阐明AP的不同发病机制和开发新的治疗方案,并了解疾病。虽然对人类胰腺的研究仍然具有挑战性,但AP的动物模型可能有助于阐明疾病的病理生理学并为开发新疗法发现新的靶点选择。本文就AP诊断和治疗相关的几个方面进行综述,并对不同的AP动物模型进行综述。
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审稿时长
12 weeks
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